Fig. 16.43 ). The •Fig. 16.44 A, Leftventricularpressure-volumeloopsrecordedinahuman.Theleftventriclewassubjectedtodifferentpreloadsbytransientocclusionofbloodflowintheinferiorvenacava.Aspreload(leftventricularend-diastolicpressure[LVEDP])wasdecreased,bothend-diastolicvolumeandend-systolicvolumedecreased,butend-diastolicvolumedecreasedmore,whichresultedindecreasedstrokevolume.B, CardiacfunctioncurveswhenstrokevolumeisplottedasafunctionofLVEDPforanormalheartinthebasalstate(blue line), aheartwithincreasedcontractility(red line), andaheartwithreducedcontractility(green line). Atanygivenpreload,strokevolumeishigherinheartswithincreasedcontractilityandlowerinheartswithdecreasedcontractilitythanstrokevolumeinthenormalbasalstate.(A, FromSenzakiH,etal.Single-beatestimationofend-systolicpressure-volumerelationinhumans.Anewmethodwiththepotentialfornoninvasiveapplication.Circulation. 1996;94[10]:2497-2506.) approximate “diastolic” arterial blood pressure may be read when the aortic valve opens (point D), and the approximate “systolic” arterial blood pressure is read during systole (point E). Left ventricular P-V loops recorded from a human (
Fig.
16.44A ) are similar to the schematized version (see
Fig.
16.43 ). The slope of the end-systolic P-V relation (line extending from the dot in
Fig. 16.44A ) defines contractility; a steeper slope indicates increased contractility. In this subject, partial occlusion of the inferior vena cava reduced the preload of the left ventricle on successive beats (as the inflow of blood to the left ventricle was reduced, as a consequence of the reduced return of blood to the right ventricle) and the effect was successively smaller stroke volume of the left ventricle.
This illustrates, in humans, the operation of the Frank-Starling law of the heart (
Chapter 13), whereby changes in preload (left ventricular volume) change myocardial fiber length, and thus the strength of the subsequent contraction, as well as stroke volume produced. This important phenomenon is characterized by the cardiac function curve (see
Fig. 16.44B).
As preload increases, stroke volume increases (solid blue line). If contractility of the heart is increased, as in the action of norepinephrine, the slope of the end-systolic P-V relation becomes steeper, and the entire cardiac function curve shifts upward (solid red line), which reflects the fact that the ventricle is now able to produce a larger stroke volume at a given preload. The increased stroke volume at any given preload is largely produced by a decreased end-systolic volume: Hearts with increased contractility are able to “squeeze down” to a greater extent. Conversely, if the ventricle is damaged, as after cardiac ischemia, or if its contractility is otherwise reduced from normal (as after calcium channel blockade), the cardiac function curve is shifted downward (green line), which reflects a reduced stroke volume at any given preload. The cardiac function curve is also known as ventricular function curves or Starling curves. To assess the integrated functioning of the cardiovascular system ( ), cardiac output, rather than stroke volume, is usually measured; preload of the heart is considered to be the filling pressure of the right ventricle, typically measured as mean right atrial pressure (Pra), or central venous pressure.
Measurement of Cardiac Output
The Fick Principle
In 1870 the German physiologist Adolph Fick contrived the first method for measuring cardiac output in intact animals and people. The basis for this method, called the Fick principle, is simply an application of the law of conservation of mass. The principle is derived from the fact that the quantity of O2 delivered to the pulmonary capillaries via